Regional blood flow and vascular resistance during hypothermia in dog

1961 ◽  
Vol 201 (3) ◽  
pp. 485-491 ◽  
Author(s):  
Bjorn Westin ◽  
N. Sehgal ◽  
N. S. Assali
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sine Wave ◽  
Blood Flows ◽  
Femoral Blood Flow ◽  
Regional Vascular Resistance ◽  
Femoral Blood ◽  
Carotid Flow

Changes in regional blood flow and regional vascular resistance during hypothermia in dogs with intact or abolished shivering mechanisms were measured with sine-wave electromagnetic flowmeters. In animals with shivering intact, cooling produced a fall in renal and carotid blood flows, despite a rise or no change in cardiac output. The fall was caused by an increase in renal and carotid vascular resistances. Femoral blood flow increased because of a decrease in vascular resistance. In animals with shivering abolished, cooling evoked a fall in the cardiac output and in renal and femoral blood flows, due to an increase in the vascular resistance. Upon rewarming, femoral flow immediately rose to values far above control. Carotid flow increased during cooling because of a decline in carotid resistance. Such a decline might have been related to the elevated blood Pco2 observed in the nonshivering animals.

Regional blood flow and vascular resistance in response to oxytocin in the pregnant sheep and dog

1961 ◽  
Vol 16 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
N. S. Assali ◽  
L. Holm ◽  
H. Parker
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Uterine Blood Flow ◽  
Pregnant Uterus ◽  
Blood Flows ◽  
Uterine Contractions ◽  
Intravenous Drip ◽  
Pregnant Sheep ◽  
Regional Vascular Resistance

The effects of oxytocin on regional blood flow and regional vascular resistance were investigated in a group of pregnant ewes and bitches not in labor and in another group in early labor. Single injections or intravenous drip infusion did not change significantly arterial pressure, cardiac output, electrocardiogram, and renal, iliac, femoral, and carotid blood flows in any of the animals studied. The effects on the pregnant uterus were negligible before the onset of spontaneous labor. Only when the animal was in labor did oxytocin produce an increase in uterine contractions accompanied by a significant decrease in uterine blood flow. The data indicate that in the pregnant sheep and dog the circulatory action of oxytocin is limited to the pregnant uterus in labor and that the decrease in blood flow is probably due to an increase in intramural vascular resistance caused by the contracting myometrium around the uterine arterioles. Submitted on May 5, 1961

Effect of K ATP + channel inhibition on total and regional vascular resistance in guinea pig pregnancy

1998 ◽  
Vol 275 (2) ◽  
pp. H680-H688 ◽  
Author(s):  
Linda Keyes ◽  
David M. Rodman ◽  
Douglas Curran-Everett ◽  
Kenneth Morris ◽  
Lorna G. Moore
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Guinea Pig ◽  
Vascular Resistance ◽  
Coronary Vascular Resistance ◽  
Ang Ii ◽  
Channel Activity ◽  
Vasoconstrictor Response ◽  
Regional Vascular Resistance

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the [Formula: see text]channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) ( n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that [Formula: see text] channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments[Formula: see text] channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased[Formula: see text] channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

Role of EDRF in the regulation of regional blood flow and vascular resistance at rest and during exercise in conscious dogs

1994 ◽  
Vol 77 (1) ◽  
pp. 165-172 ◽  
Author(s):  
W. Shen ◽  
M. Lundborg ◽  
J. Wang ◽  
J. M. Stewart ◽  
X. Xu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Skeletal Muscles ◽  
Acute Exercise ◽  
Regional Blood Flow ◽  
Conscious Dogs ◽  
Tissue Blood Flow ◽  
Minor Role ◽  
Blood Flows ◽  
A Minor

The contribution of endothelium-derived relaxing factor (EDRF) to the regulation of regional vascular resistance and tissue blood flow at rest and during acute moderate exercise was studied in chronically instrumented conscious dogs. Radioactive microspheres were injected before and during exercise to measure regional blood flow. An infusion of nitro-L-arginine (L-NA), an analogue of L-arginine, was used to inhibit the synthesis of EDRF and resulted in a significant increase in mean arterial pressure, associated with significantly elevated vascular resistance in heart, skeletal muscle, renal and splanchnic circulations and with decreases in tissue blood flow in those regions at rest. Acute exercise caused a typical redistribution of blood flow, in which there was vasodilation in heart and working skeletal muscles, accompanied by vasoconstriction in kidney and splanchnic circulations. L-NA resulted in significantly elevated vascular resistance during vasodilation in heart and working skeletal muscles and also significantly increased vasoconstriction in renal cortex, stomach, pancreas, liver, and colon during exercise. Blood flows during exercise were largely unaffected by L-NA treatment. Our results suggest that whereas EDRF functions to regulate basal vascular tone and vascular resistance during exercise, EDRF has a minor role in determining the pattern of the redistribution of tissue blood flow during exercise.

Hemodynamic and histomorphometric characteristics of dilated cardiomyopathy of Syrian hamsters (Bio TO-2 strain)

2001 ◽  
Vol 79 (4) ◽  
pp. 329-337 ◽  
Author(s):  
Sonia Goineau ◽  
Danielle Pape ◽  
Pascal Guillo ◽  
Marie-Paule Ramée ◽  
Eric Bellissant
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Computer Assisted ◽  
Image Analyzer ◽  
Hepatic Congestion ◽  
Femoral Blood Flow ◽  
Cardiomyopathic Hamsters ◽  
History Of ◽  
Computer Assisted Image ◽  
Femoral Blood

The natural history of the disease of the dilated strain Bio TO-2 of cardiomyopathic hamsters (CMH) is not totally characterized. We investigated its hemodynamic and histomorphometric characteristics at 140, 180, 220, 260, and 300 days of age. Forty CMH and 40 controls were investigated (8 at each stage). Mean arterial pressure (MAP, carotid artery catheter) and cardiac output and femoral blood flow (CO, FBF, transit time method) were measured in anesthetized animals. Systemic (SVR) and femoral (FVR) vascular resistances were calculated. Atria, left and right ventricles (LV, RV), lungs, and liver were weighed. LV cavity area, LV and RV wall thicknesses and collagen densities were determined (computer-assisted image analyzer). Pulmonary and hepatic congestion were assessed (arbitrary scales). Compared with controls, MAP, CO and FBF were significantly lower in CMH throughout the study (on average: –22%, –34%, –33%, respectively), FVR was significantly increased (+15%), but SVR was not significantly modified. Concerning histomorphometric characteristics, differences between groups significantly increased with age for most variables: at 300 days, atria (+292%), RV (+13%), lungs (+44%), and liver (+23%) weights, LV cavity area (+130%), LV (+364%) and RV (+181%) collagen densities were significantly increased in CMH vs controls, whereas LV (–40%) and RV (–23%) wall thicknesses were significantly decreased. At 260 and 300 days, CMH showed significant pulmonary congestion without hepatic alteration. Bio TO-2 CMH progressively develop an alteration of cardiac function leading to decreased MAP and musculo-cutaneous blood flow associated with cardiac remodeling including atria hypertrophy and LV dilation, wall thinning and a rise in collagen density.Key words: cardiomyopathy, heart failure, regional blood flow, remodeling.

Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR

1985 ◽  
Vol 249 (6) ◽  
pp. R781-R786 ◽  
Author(s):  
R. W. Lappe ◽  
J. A. Todt ◽  
R. L. Wendt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Sympathetic Nerves ◽  
Spontaneously Hypertensive ◽  
Regional Vascular Resistance ◽  
6 Hydroxydopamine ◽  
Renal Vascular ◽  
Renal Sympathetic

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.

Fever and regional blood flows in wethers and parturient ewes

1988 ◽  
Vol 65 (1) ◽  
pp. 165-172 ◽  
Author(s):  
C. M. Blatteis ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
T. A. Mashburn
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Full Term ◽  
Blood Flows ◽  
Pregnant Sheep ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Placental Blood Flow

To determine whether the reported absence of fever in full-term-pregnant ewes might be associated with shifts of regional blood flows from thermogenic tissues to placenta during this critical period, fevers were induced twice by injections of Escherichia coli lipopolysaccharide (LPS, 0.25 microgram/kg iv) into each of six Merino ewes from 8 to 1 days prepartum, and their regional blood flow distribution was measured with radioactive, 15-microns-diam microspheres before and during the rise in fever (when their rectal temperature had risen approximately 0.4 degree C). Unexpectedly, fever always developed, rising to heights not significantly different at any time before parturition [4-8 days prepartum = 0.81 +/- 0.23 degree C (SE); 1-3 days prepartum = 0.75 +/- 0.17 degree C) and similar to those in three wethers treated similarly (0.90 +/- 0.10 degree C). Generally, during rising fever, blood flow in the ewes shifted away from heat loss tissues (e.g., skin, nose) to heat production tissues (e.g., shivering muscle, fat) and cardiac output increased; blood flow through redistribution organs (e.g., splanchnic bed) decreased. The reverse occurred during defervescence. Utero-placental blood flow remained high in the febrile ewes. These regional blood flow distributions during febrigenesis and lysis are essentially the same as those during exposures to ambient cold and heat, respectively. Some differences in the responses of cardiac output and its redistribution, however, were apparent between wethers and pregnant ewes. We conclude that 1) the previously reported "absence of fever in the full-term-pregnant sheep" should not be regarded as a general phenomenon and 2) full-term-pregnant sheep support fever production without sacrificing placental blood flow.

Peripheral vasodilatation induced by a vasopressin analogue with selective V2-agonism in dogs

1989 ◽  
Vol 256 (6) ◽  
pp. H1621-H1626 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Hemodynamic Effects ◽  
Femoral Blood Flow ◽  
Peripheral Vasodilatation ◽  
Femoral Blood

The selective V2-agonist 4-valine-8-D-arginine vasopressin (VDAVP) increases cardiac output and heart rate and decreases total peripheral resistance in dogs. The mechanism of these hemodynamic effects was examined in the present studies. When infused into the left coronary artery of six conscious dogs for 1 h, VDAVP (10 ng.kg-1.min-1) increased cardiac output and decreased total peripheral resistance more than when given intravenously in the same animals. Administration of VDAVP into the carotid circulation elicited effects that did not differ significantly from those after intravenous infusion at the same rate in six conscious dogs. After destruction of the central nervous system in five dogs anesthetized with pentobarbital, VDAVP failed to increase cardiac output and heart rate but lowered mean arterial pressure and total peripheral resistance. Finally, infusion of VDAVP into the femoral artery of six anesthetized dogs increased femoral blood flow at rates of 1, 5, and 10 ng.kg-1.min-1, whereas none of these rates increased femoral blood flow when given intravenously. Thus the hemodynamic effects of VDAVP appear to result primarily from a peripheral vasodilatory action, with possible contribution from a positive inotropic effect. We found no evidence that central effects of VDAVP were importantly involved in its cardiovascular action.

Effects of exercise, hypoxia and feeding on the gastrointestinal blood flow in the Atlantic cod Gadus morhua

1991 ◽  
Vol 158 (1) ◽  
pp. 181-198 ◽  
Author(s):  
M. Axelsson ◽  
R. Fritsche
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Mesenteric Artery ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Control Mechanisms ◽  
Artery Blood Flow ◽  
Blood Flows ◽  
Mesenteric Artery Blood Flow

Cardiac output, ventral and dorsal aortic blood pressure, heart rate, and coeliac and mesenteric artery blood flow were recorded simultaneously in the Atlantic cod, Gadus morhua L., at rest, during exercise, during hypoxia and after feeding. In the resting unfed animals, coeliac artery blood flow was 4.1 +/− 0.8 ml min-1 kg-1 and mesenteric artery blood flow was 3.5 +/− 1.1 ml min-1 kg-1 (mean +/− S.E.M., N = 10); together, these flows represent approximately 40% of the cardiac output. Exercise or exposure to hypoxia resulted in increased visceral vascular resistance, leading to reductions in the coeliac and mesenteric artery blood flows. Coeliac and mesenteric blood flows were increased 24 h after feeding and the coeliac and systemic vascular resistances decreased in comparison with the prefeeding values. Phentolamine did not affect the gastrointestinal artery blood flow, but produced a significant decrease in the mesenteric and systemic vascular resistance. Treatment with bretylium and phentolamine revealed differences between the coeliac and the mesenteric vasculature regarding the control mechanisms during hypoxia and during exercise and feeding. During hypoxia, an adrenergic control of the gastrointestinal vasculature with both nervous and humoral components was found, whereas during exercise and after feeding an additional non-adrenergic mechanism controlling gut blood flow was demonstrated.

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